Developmental
Toxins, Carcinogens, and Mutagens and their Concentrated Presence in Breast
Milk

Note: Much of the information in this
section is somewhat technical, and it is rather lengthy. As an
introduction to it, we will begin with a brief presentation of some specific
points about why people should be re-examining their positions on
breastfeeding, and will then touch briefly on information about infant exposures
to toxins as well as apparent effects of the toxins of concern.

The U.S. Surgeon General acknowledges
that "research on the health outcomes of different modes of infant feeding
is limited to observational studies, the results of which can only provide
inferences...."1 Because of
"confounders" (underlying, actual causes of the associations
found in studies), the U.S. Agency for Healthcare Research and Quality
points out that observational studies are subject to "false
conclusion."2

Norway is at the very top level of the
world's long-standing high-breastfeeding countries.3 There is
therefore extra credibility in a statement about effects of breastfeeding if it
is made by researchers from the Norwegian University of Science and Technology,
especially when they are summarizing "the largest
study that has been done on breastfeeding and health." That
study was apparently also the only breastfeeding study that has utilized
randomization, the best way to avoid effects of confounders. Their
statement was as follows: "This study cuts the legs out from
underneath most of the assertions that breastfeeding has health benefits."4

* * * * * * * * * * * * * * *

Many scientific studies have
found that health outcomes are worse among children who were more
breastfed than among children who were breastfed less or not at all, with at
least 26 such studies in the categories of asthma, allergies and diabetes
alone, three regarding autism, and one finding a dose-response relationship
between toxins in breast milk and behavior scores in the breastfed children
indicating likelihood of later having ADHD.5

* * * * * * * * * * * * * * *

Average daily exposure of a breastfed
infant to dioxin toxicity over
the period of a year, as estimated by the EPA, is over 80 times
higher than the reasonably-safe upper threshold of dioxin exposure estimated by
the EPA.6

* * * * * * * * * * * * * * *

The Danish scientist who is author of
nine studies on chemical contamination of human milk and 40 other studies, as
well as Head of the Section of Environmental Technology of the Danish Institute
of Technology, said,"The average levels of persistent
organohalogens in human milk are normally 10 to 20 times higher than the levels
in cow's milk or infant formulas." 7Organohalogens include dioxins,
PCBs and PBDEs, all of which are neuro-developmental toxins;
all of them are also part of diesel emissions.8 Note that diesel emissions were
one of only two pollutants that were most strongly implicated in the 2013
Harvard study that found close correlations between autism diagnoses and
environmental pollution at the times and places of the children's births.9

* * * * * * * * * * * * * * *

A U.S. study of all 50 U.S.
states and 51 U.S. counties, carried out by a highly published scientist and
Fellow of the American College of Nutrition, found that "exclusive
breast-feeding shows a direct epidemiological relationship to autism" and
also, "the longer the duration of exclusive breast-feeding, the greater
the correlation with autism."10

Two other studies, in the U.S. and
U.K., came to conclusions similar to the above, with a dose-response
relationship between breastfeeding and autism indicated by comparing the
findings of the two studies.11

* * * * * * * * * * * * * * *

"Overwhelming evidence" (as
stated by the UCLA Food & Drug Allergy Care Center) suggests that "the
hygiene hypothesis explains most of the allergy epidemic."12
According to that, there are too few microbial challenges in our current
environments in developed countries to properly stimulate development of the
immune system. So the undisputed immune cells in breast milk are further
reducing challenges that apparently already have become too low for
proper development of children.

* * * * * * * * * * * * * * *

In the decades following the major
increase of U.S. breastfeeding rates beginning in the 1970's, not one of the
disorders alleged by Surgeon General Regina Benjamin to be reduced by
breastfeeding declined, as indicated by data from the CDC and other authoritative
sources. In fact, all but one actually increased substantially, often in
precise correlation with major variations in the breastfeeding rate increases.13

* * * * * * * * * * * * * * *

There is one piece of advice about
breastfeeding from earlier decades that still has validity, which is that
lactation reduces a woman's body burden of persistent toxins (by means of
excreting those toxins in breast milk); and it therefore might reduce
her risk of cancer. But, seeing the extremely close correlations between
breastfeeding rates and incidences of childhood cancer14 as well as
autism, some mothers are starting to question whether it is desirable to
transfer those toxins to their rapidly-developing babies at the most vulnerable
times of the infants' lives.

*
* * * * * * * * * * * * * *

Criticisms of any of the points above
are earnestly requested, if you feel that anything said is not an accurate
representation of information from authoritative sources (see sources below).Our intention is to make this
website as accurate as possible. Please make any comments specific
regarding any statements you consider not to be accurate in relation to the
sources. Or indicate why any sources indicated are not trustworthy.
Please send any responses to dm@pollutionaction.org , and they will be posted
below. Thank you for your attention to this important matter.

The compete presentation about toxins in breast milk
and formula, and their effects will follow right after this set of
footnotes.

(3) See www.breastfeeding-rates.info,noting
Norway's 6-month rate in the Europe chart and then seeing the 6-month
breastfeeding rates in the World data set, with only Mongolia and Rwanda
sharing the top position.

(4) "Breastfeeding is not as beneficial as
once thought" (06.01.2010) published by the Norwegian University of
Science and Technology, at http://www.ntnu.edu/news/breastfeeding Their statement was
based on findings of the PROBIT study in Belarus. (This article, on the website
of the Norwegian
University of Science and Technology, indicated no author; it therefore
appears to be an established, official statement of the University, dated 2010
and accessed in 2013.)

Also www.epa.gov/iris/supdocs/dioxinv1sup.pdf in section 4.3.5, at end of
that section, "...the resulting RfD in standard units is 7 × 10−10
mg/kg-day." (that is, O.7 pg of TEQ/kg-d) In the
EPA’s “Glossary of Health Effects”, RfD is defined: “RfD (oral reference
dose): An estimate (with uncertainty spanning perhaps an order of magnitude) of
a daily oral exposure of a chemical to the human population (including sensitive
subpopulations) that is likely to be without risk of deleterious noncancer
effects during a lifetime.”

(7) Jensen, A.A. et al, Chemical
Contaminants in Human Milk, CRC Press, Inc., Boca Raton, Ann Arbor, Boston,
1991, p. 287. (Many libraries would not have this, but it should be available
as an Inter-Library Loan.)

(11)
Breastfeeding and Autism P. G. Williams, MD, Pediatrics, University of
Louisville, and L. L. Sears, MD, presented at International Meeting for Autism
Research, May 22, 2010, Philadelphia Marriot, found at https://imfar.confex.com/imfar/2010/webprogram/Paper6362.html) The percent of
ASD-diagnosed patients who had been breastfed at 6 months was 37%, as
compared with 13% in the control group (or 14% in the general Kentucky
population). Also Trends in Developmental, Behavioral and Somatic Factors by
Diagnostic Sub-group in Pervasive Developmental Disorders: A Follow-up
Analysis, pp. 10, 14 Paul Whiteley (Department of Pharmacy, Health
& Well-being, Faculty of Applied Sciences, University of Sunderland, UK),
et al. Autism Insights 2009:1 3-17 at http://www.la-press.com/trends-in-developmental-behavioral-and-somatic-factors-by-diagnostic-s-article-a1725) Also: Patterns
of breastfeeding in a UK longitudinal cohort study, Pontin et al., School of
Maternal and Child Health, University of West of England, Bristol, UK.
The records showed that 65% of the children with those conditions
had been “exclusively breastfed” for over four weeks. After doing a
search of available sources for a comparison figure for exclusive breastfeeding
for over four weeks for the U.K. as a whole for the period in which those
children would have been newborns, this author has come up with data from two
different sources, which are consistent in leading to a figure of about
28%. This is a lower ratio of cases to general population compared with
the Williams study, in a study in which the duration of the breastfeeding being
compared was also lower than in the Williams study.

And
now the details about toxins in breast milk and formula, and their effects:

In the words of the U.S.
Agency for Toxic Substances and Disease Registry, with emphasis added:
"The proper development of many systems and functions (in an
infant) depends on the timely action of hormones...; therefore,
interfering with such actions can lead to... altered metabolic, sexual, immune, and neurobehavioral functions. Effects of this
type...occur following exposure....early in life caused by either direct
exposure to chemicals or exposure (to environmental
chemicals)via maternal milk."(28)(The text segments that applied
directly to the present discussion were selected from the original text;
the complete text can be found at the footnote shown.)

How
these chemicals cause harm:
One important form of dioxins is a known carcinogen, other forms of
dioxins are classified as likely carcinogens, and PAHs are well known to
cause cancer in animals.28a One specific
means by which dioxins, BPA and at least one PAH cause neuro-developmental
harm is by acting as "endocrine disruptors." A web
page of the National Institutes of Health says that endocrine disruptors are
"chemicals that may interfere with the body’s endocrine system and produce
adverse developmental,reproductive,neurological, and immune
effects in both humans and wildlife. …. ." (emphasis added)
Some PAHs have been identified as mutagens, which can have adverse
effects on the ways organs including the brain develop.

Quoting from the NIH's web
page on endocrine disruptors, "Endocrine
disruptors …may mimic or interfere with the function of hormones in
the body. Endocrine disruptors may turn on, shut off,
or modify signals that hormones carry,…" (emphasis added) (30)Continuing,
"Research shows that endocrine disruptorsmay pose thegreatest risk during prenatal
andearly postnatal development when organ and neural systems are developing. According to the Committee on
Developmental Toxicology of the National Academy of Sciences, ”Agents that
interact with one or more of these receptors and are known
to produce abnormal development
include ……dioxin (TCDD)." Explaining how
dioxin affects the developing body, the NAS committee points out that
it "... alters the expression of several dozen
genes, one or more of
which mightresult
in an adverse developmental
outcome." (31) (emphasis added)

Sources of these toxins: The
EPA's web pages and documents on dioxins and PAHs point out major sources of
dioxins and PAHs as follows: (a) dioxins are unintentional
byproducts of several industrial chemical processes and of most
forms of combustion, including wildfires, backyard burning, municipal solid waste and industrial and hospital
incineration,vehicle
exhaust (mainly diesel emissions), and emissions from oil- or coal-firedpower
plants, and are also
found in weed killers and in ordinary soil onto which dioxins have settled and
been precipitated out of the atmosphere; (b) PAH's are also
unintentional products of typical forms of combustion,
including cigarette smoking, residential wood burning and vehicle
emissions.(34) (Note that most of
the above sources are related to population density and combustion
processes.) Animal fat in the diet accounts for close to 90%
of dioxinexposure in the United States,
according to a 2003 National Academies of Science report on dioxins in the food
supply. (34a)Vegetarians are reported to consume
only 2 percent of the dioxin load of the general population, because their diet
is dominated by foods low on the food chain. (34d)Most human intake of PBDEs
comes from dust released by electronic devices within homes and buildings.
Human exposure to BPAs comes mainly from plastic
packaging of food and metal cans.

The
predominant source of high doses of these toxins to
infants:

To provide
an idea of how much dioxin is a significant hazard to human infants, note that
(in its most recent dioxin assessment, issued February, 2012), theEPA
set the threshold for safe dioxin exposure at a toxicity equivalence
(TEQ) of 0.7picograms
per kilogram of body weight per day.(34b) Note that what appears to be
the only EPA estimate of infant exposure to dioxins predicts that an
infant breastfed for one year would receive an average daily dose of about 60
pg of TEQ/kg bw/day.(34c)So the average daily dose of 60 pg, over
the period of a full year of rapid development, is 86 times the estimated
safe dioxin exposure of 0.7 pg.

The above figures are estimated average
daily exposures over a full year of breastfeeding, taking into account the
lower levels that occur later in the year during the course of excretion by way
of lactation. The peak body-weight-based dose received by a
breastfeeding infant is estimated in an EPA study to be 242pg TEQ/kg-day.(37a) Note that these extremely
unsafe exposures of breastfed infants come at the most vulnerable times of
their lives for neurological development, and they come shortly before a
high-level period for development of childhood cancer. (see www.breastfeeding-and-cancer.info)

Concentration
of toxins in breast milk, causing many-times higher infant intake than from
formula or from trans-placental exposure:

According to the U.S. Agency for Toxic
Substances and Disease Registry (ATSDR), ”PCBs
tend to accumulate in breast milk fat,” with accumulations increasing with
the woman’s age. (82a) A study cited by the ATSDR
showed the intensity of concentration of PCBs in breast milk:
“Daily PCB intake for native northern Quebec women was calculated to be
0.3 μg/kg (ppb) body weight while daily intake among infants was
calculated to be 10 μg/kg due to breast feeding.”(Section
6, p. 584)That
means that, at least as found in this study,toxins that enter the
woman’s body are excreted in breast milk in what is effectively a
30-times-higher concentration compared with their entering concentration. A
study in the Netherlands, also summarized by the ATSDR (p. 569), found that, at
42 months of age, the median plasma PCB levels of children who had been
breastfed for at least 6 weeks were 4½ times as high as those of children who
had been formula-fed.

The
above two comparisons implied the nature of, but didn't specify, the ratio of
PCBs taken in by a breastfed infant compared with the intake of an adult.
A figure for that is provided by a commission of the German Federal
Environmental Office, which reported that the average daily intake of an adult
is 0.02 micrograms of PCBs per kg of body weight, as compared with the intake
of a breastfed infant, which is 3 micrograms per kg of body weight, or 150
times higher.(82c)

It might seem that growing for nine
months inside a mother's body would put a fetus at maximum vulnerability for
exposure to toxins that have accumulated in the mother, but apparently that
exposure can be minor compared with the effects of breastfeeding.
According to what is apparently the most thorough study on the subject of
infant absorption of toxins from mother's milk vs. from fetal absorption, "Significantly
more (10 to 20
times) of
a mother's body burden of persistent organohalogens is transferred to the
infant via the milk than by the transplacental route." (Note that dioxins, PCBs and PBDEs
are included among organohalogen compounds.) Tests with animals have
confirmed the above, with even higher ratios of lactational vs. transplacental
transfer. (81b)

According to an EPA report, providing
estimates for typical exposure in the U.S. based on EPA data but also drawing
on studies of populations in Germany (two studies), Britain and the
Netherlands,"Breast-feeding
for 6 months or more is predicted to result in an accumulated (dioxin)
exposure 6 times higher than a formula-fed infant during the infant's first
year of life.”. (83) A German study found thatintake
of dioxins was up to 50 times higher in breast-fed infants compared with
formula-fed, and also
that high proportions of the dioxins were intestinally absorbed by the
breastfed infants. At 11 months of age, the dioxin toxicity-equivalent concentrations
in the formula-fed infants were about10
times lower than in the infants that were breast-fedfor six to seven months. (85) This study (Abraham et
al.) was cited in a 2002 EPA document ("Infant Exposure to Dioxin-like
Compounds in Breast Milk") that apparently considered it to be fully
valid. (37a)

However,
the 6- or 10-times-higher range of long-term accumulation or concentration in
the breastfed infants may understate the reality of the harm caused, since the
"up to 50 times higher" short-term exposure may result in
unusual harm just during that short-term period; this is especially
likely to be the case since higher doses come earlier in the lactational
period, when the "window of sensitivity" for neurological development
is likely to be taking place (see Section 1.2.b.1 at www.pollutionaction.org/breastfeeding-and-autism-and-cancer.htm.

The presence of these "persistent" toxins in the child's
body declines after their rapid buildup during breastfeeding, but only very
gradually. PCB levels in children who had been breastfed for at
least 12 weeks were still over twice as high as in bottle-fed children
at 7 years of age, in an American/German study. (82b)

The
EPA's 2010 Exposure Assessment of PBDEs found an estimated total
adult intake dose of 7.1 ng/kg-day (nanograms per kilogram of body weight per
day). Comparing with various figures for other age groups,
"infant intakes due to ingestion of mother’s milk were the highest at 141
ng/kg/day." So the average effective intake of a breastfeeding
infant from mother's milk alone is 20 times the average total intake of
adults. On top of that, infants also take in far more PBDEs than
adults do from dust, and dust is by far the largest source of PBDE exposure to
the general population. (81c) In the only comparison the EPA provides
of PBDE food intake by a breastfed infant compared with food intake of PBDEs by
an average adult, the breastfed infant was estimated to take in over 200 times
as much as the adult.(81d) See farther down about
developmentally-toxic effects of PBDEs (apparently leading to greatly increased
likelihood of ADHD) and their extremely rapid increases in the environments of
developed countries in recent decades.

PBDEs
in breastfed vs. bottle-fed children:
In the only study quoted by the EPA making such a comparison, based on
measurements of 244 children (Carrizo et al., 2007), the average total concentration
in children that had been breast fed was still nearly three times as high as
average concentrations in formula-fed children at age 4(3.6
vs.1.3 ng/g lwt).(81e) This is as should be expected,
judging by the differences in PBDE concentrations found in infant formula vs.
breast milk, as follows: In the only data regarding PBDE concentrations
in infant formula that is provided in the EPA's PBDE Exposure Assessment
(citing Schechter et al., 2006 a), two samples of infant formula were found to
have PBDE concentrations of 32 and 25 pg/g wwt (wet weight),
respectively. (81f) Going by EPA data, total PBDE
concentrations in mother's milk average about 1760 pg/g wwt or higher.(81g)
Such a difference in contents of this toxin between human milk and formula is
not surprising, considering that about 90% of human intake of PBDEs comes from
dust released by electronic devices within homes and buildings, according to
the EPA; cows and soybean plants (the chief sources of alternatives to breast
milk) obviously don't live inside houses containing TVs, computers and other electronics.

Mercury (another of the "persistent,
bio-accumulative toxins" that increase greatly with each step up the food
chain) would clearly accumulate more in humans who eat fish, especially large
fish, than in cows. (The EPA says that "Nearly all methylmercury exposures in the U.S. occur through
eating fish and shellfish."(81y)) In a 2013 Harvard University
study, five environmental pollutants at time and place of birth were found to
be specifically connected with likelihood of later autism diagnosis of the
child; two were especially strongly associated with autism;
mercury was one of those two.(81w) That study's research drew on a far larger base of
data than any previous study on the subject.

According to EPA-contracted
researchers, "A wealth of information on the pharmacokinetics of Hg and
MeHg (mercury and a mercury compound) exists in the available literature
(extensively reviewed by U.S. EPA, 1997b). Together, the data indicate that the
lactational transfer of Hg during the first 15 days of lactation accounts for
roughly one-third of the transfer of Hg during gestation."(81t)Notice that, in just 15 days
of breastfeeding, an amount of mercury is transferred to the infant equal to
one third of the entire amount that was transferred during the many months of
gestation. The placenta provides some shielding of the fetus from
toxins; and ingestion in food is typically an efficient means of
absorption of toxins. Judging by the above quotation, it seems probable
that total transfer of mercury during lactation would typically be greater than
the mercury transferred during gestation.

In addition, retention
of the transferred mercury is apparently greatly increased by infant consumption
of milk or formula as opposed to solid food. A study of mercury retention
by infant monkeys found that both blood and hair mercury showed a sudden drop
directly after weaning, which was accompanied by a several-fold increase in
fecal mercury excretion."(81v) (See chart below.)

The mechanism that
causes this to take place (retention of mercury during breastfeeding, stopping
after weaning) seemed to be unknown (milk facilitating gut absorption of
ingested mercury, or solid food promoting flow of intestinal content containing
or binding to mercury?). But it appears to be clear that milk-feeding vs.
solid-food feeding makes the difference between major buildup (or continued
buildup) of mercury in the infant's body and excretion of most of the mercury.

Note that monkeys, like
humans, are primates. Since humans aren't used as laboratory animals,
what happens in monkeys' bodies probably provides the closest available
approximation of what happens inside human bodies.

Notice in this chart that most of the
brain's growth and development (especially of the cerebellum) takes place
during the first year after birth, while most breastfeeding takes
place. And note that "there is increasing recognition that the cerebellum
contributes to cognitive processing and emotional control in addition to its
role in motor coordination."(81u)

To sum up some preceding information:

Transfer of mercury to infants
by lactation is apparently much faster than during gestation. And
mercury's excretion from the infant's body is apparently greatly retarded by
milk-type feeding. Aside from mercury, 10 to 20 times as much of a
mother's body burden of organohalogens (heavily present in diesel emissions)
is transferred to the infant in breast milk than is transferred during
gestation. (see above) Remember also from earlier that mercury and diesel
emissions are the two environmental pollutants that were identified in a
2013 Harvard study as being most closely linked to incidence of autism.

Milk is far higher in mercury in
lactators who eat fish and have amalgam fillings (i.e., human mothers) than in
those that don't (i.e., cows); and organohalogens are many times higher
in human milk than in cow's milk or formula (see above). So both of the
two specific pollutants that have been most closely implicated with likelihood
of autism become greatly increased in the infant by breastfeeding.

Consider the above in relation to the
fact that most of the brain's growth and development takes place during the
first year after birth (see chart above/right).

Also consider all of the above in
relation to the finding by a highly-published scientist and Fellow of the
American College of Nutrition, concluding a U.S. study of all 50 U.S. states
and 51 U.S. counties, that "exclusive breast-feeding shows a direct
epidemiological relationship to autism" and also,"the
longer the duration of exclusive breast-feeding, the greater the correlation
with autism."(81x)

...........................................................

In order to appreciate the fact that typical
breast milk in nursing mothers these days is very different from that of
earlier times,
one should be aware of the following:

Dioxins:

1) Estimates from various studies
suggest that rates of dioxin deposition in the environment (mostly from the
air) increased
more than 10-fold
between the 1930s and the late 1960s. (86) Smokestack sources of
dioxins have declined recently, but sources in the U.S. that reach
populated areas intensively (dioxins in diesel emissions) have continued to
greatly increase, as of the most recent data;(96) and those "persistent"
toxins continue building up in the environment, especially in soil (and from
there back into the air, water and food supply). Remember from earlier how
far dioxin contents of typical breast milk have been found by the EPA to exceed
the EPA's estimated safe level, and also bear in mind from just-preceding
paragraphs how far a breastfed infant's ingestion of dioxins exceeds that of an
infant that has not been breast fed.

2) The average dioxin
content per ounce of animal-based foods is much higher than in earlier times, following the increases of toxins in
the environment. The U.S. Agency for Toxic Substance and Disease Registry
says that "eating food, primarily meat, dairy products, and
fish, makes up more than 90% of the intake
of CDDs (dioxins) for the general population." (88) Farm animals and fish ingest
and build up persistent toxins in their tissues largely as a result of what
they eat, meaning vegetation and sediment onto which the greatly-increased
levels of dioxins and mercury from the environment have been deposited;
in addition there is"bio-magnification" as the increasing accumulated
concentrations of toxins in animal tissues and dairy products(especially in the fat content) are
passed up the food chain (via smaller fish being eaten by larger fish, and
animal-based products being eaten by humans).

3)"Meat
consumption has more than doubled in the United States in the last 50 years,"(89) while the population only
increased 72%.

Heavy metals:

Other neurological toxins
or carcinogens of concern are contained within breast milk. Quoting from
page 12 of an IFCS FSC Working Group paper,"Heavy metals such as methylmercury and leadare also secreted in breast milk."According to the EPA, mercury in
the ­atmosphere tripled between the era before human activity and
current times,(254)
and it continues to increase moderately rapidly, coming from many
combustion sources (especially coal-fired power plants).

PBDEs:

PBDEs didn't come into use
until the 1960's and 1970s. (245b) They are
essentially used as fire retardants in consumer plastics, especially electronic
devices such as TVs and computers. According to a Japanese study,
"Several toxic effects on the thyroid
system
or on neurodevelopment have been reported in experimental animals exposed to PBDEs."(90)Note in Section 1.2.b.1 at this link that increases or
decreases in thyroid levels have been reported to "cause irreversible neurological damage" during development
of the brain. Also note in Section 1.7.1 at this link about endocrine-disrupting, anti-androgenic,testosterone-reducing effects of PBDEs, which could well be already at toxic levels according
to the EPA, even while levels in humans are rapidly increasing.And remember from earlier
that a breastfeeding American infant receives a dosage of PBDEs from mother's
milk alone that is about 20 times as high as the total average adult
intake. Remember also that current exposure to PBDEs alone is
likely sometimes to be at toxic levels, not to mention the other toxins that
are also known to be present in breast milk

Diesel emissions:

Remember that the dioxin component of
diesel emissions in the U.S. approximately doubled in the last
13-year period for
which the EPA provides data.(96)
(Bear in mind from earlier that dioxins in breast milk are known to especially
greatly exceed the safe level estimated by the EPA. Considering that
dioxins from diesel emission have been rising greatly, it should be safe to
assume that diesel emissions in general have also been increasing
substantially. Note that diesel engine exhaust was classified as a known
human carcinogen by
the EPA in 2012. One of the other toxic components known to be
contained in the rising diesel emissions, PAHs (known
to cause cancer in
animals), has almost certainly also continued to increase in atmosphere inhaled
by many nursing mothers and mothers-to-be. Note in the next
paragraph how closely PAH concentrations in breast milk are related to exposure
to diesel exhaust.

The chart on the left (from a Japanese study) indicates high concentrations of

five different kinds of PAHs in breast milkof rats that had been exposed to

diesel exhaust (DE) for six hours a day from the seventh day of gestation until

14 days after birth, with concentrations similar to those in downtown

Kanazawa, Japan37b (Kanazawa is the study's lead author's university city,

population 450,000). PAH concentrations in the breast milk of the exposed

rats ("DE") were two to three times higher than in the control group,despite

the fact that the exposure was apparently only moderately high; note that this

exposure of

the rats to diesel exhaust, for only six hours a day, was not an especially high

dosage. As indicated in this chart, lactation appears to be an efficient means

of taking in toxins from the atmosphere and concentrating them in breast milk.

Although information about PAHs in cow's milk does not appear to be available

for comparison, it is probably safe to assume that a much higher percentage of human

mothers and mothers-to-be than of cows has a close exposure to diesel exhaust, from

An Italian study found PAHs
to be higher in lactating women who smoke. The specific form
of PAH that was investigated in this study was benzo(a)pyrene (BaP),
which is classified as a Class 1 carcinogen by the International Agency
for Research on Cancer. There is no determination of a maximum tolerable
amount in breast milk, so the Acceptable Daily Intake
(ADI) for drinking water was used in the study. "For babies whose mothers
belonged to the non-smoker rural category, daily BaP equivalent intake
during a six-month nursing period was below the ADI." But
intake of BaP in breast milk by infants of urban smokers showed values
"from about seven times, up to 1000 times higher than ADI."
(emphasis added) Breast milk of urban non-smokers was intermediate in
concentrations.(26a)Note that BaP is also a major
component of diesel exhaust,(90c) as well as of tobacco smoke.

Authorities writing about
dioxins, which are better known than PAHs, emphasize the predominant role of
diet as being the major source of those toxins into the body (and thereby into
breast milk). It is worth taking special note of the fact that, in the
cases of the also-toxic PAHs from diesel exhaust and tobacco smoke (as
indicated above) and also PBDEs from electronics,the inhalation route is also an
important means of absorbing environmental toxins which can then become
concentrated in breast milk. In
that regard, remember from earlier that PAHs are not only carcinogens but also
endocrine disruptors, capable of damaging neurological development. Then
note that a study of effects of proximity to California freeways (published in
2011) found a doubled percentage of autism among
infants residing within about 1000 feet of freeways, compared with those
farther away.(194)

The
above two studies appear to be the only ones published regarding presence in
breast milk of PAHs (including BaP). They show carcinogens
and probable developmental toxins being found especially concentrated in breast
milk following rather ordinary exposures of the mothers to diesel emissions and tobacco
smoke. The amount of PAHs in the breast milk was directly related to the
extent of the mothers' exposures to the chemicals. The finding of carcinogenic
intake of BaP by breastfeeding being up to 1000 times the acceptable level for
infants of urban smoking mothers, while levels were in the safe range for rural
non-smokers, highlights how extremely effective
lactation is at taking in environmental pollutants in typical amounts and
concentrating them in breast milk.

Mothers
should not necessarily feel safe about their breast milk if they are rural
non-smokers. Whereas PAH's are apparently mainly taken in by inhalation, dioxins
are mainly taken in by way of food;
unless one lives in
an unusually low-pollution food-source region, the only way to avoid typical
concentrations of dioxins in breast milk is to adopt a basically vegetarian
diet many years before breastfeeding starts. Also, residential
wood-burning emissions are a major source of BaP(26b)and particulate matter, and a
significant source of lead, typically emitted in the immediate air supply of
both lactating mothers and infants. Breast milk in rural Italian mothers was
probably uniformly within acceptable limits of BaP at least partly because
there is relatively little residential wood burning in sunny Italy, with
minimal forests. It is also important to bear in mind that backyard
burning, often done in rural areas, has become the largest single source of
releases of dioxins to the atmosphere in recent years, according to the
EPA. In addition, high levels of PBDEs in breast milk apparently result
mainly from exposure of mothers to air around electronic devices. (See earlier
in this section.)

One can be safe in assuming
that most cows do not have nearly the exposure to diesel emissions, tobacco
smoke, air surrounding electronic devices, and residential wood-burning
pollution that human mothers have, not to mention not eating meat, fish and
dairy products into which toxins have bio-accumulated.

Continuing
increases of developmental toxins in environments of developed countries:

The EPA reports that major
smokestack sources of dioxins in the atmosphere have declined greatly in
recent decades as a result of regulatory efforts, but dioxins are extremely
persistent in the environment, especially in soil; and releases of dioxins indiesel emissions(which often reach heavily at ground level into
highly-populated areas)have continued to increase rapidly, as of the most recent
EPA data (for year 2000). It is probable that diesel emission pollution
will continue to increase in the U.S., as more and more decades-old
diesel-powered vehicles continue in operation in the U.S. without emission
restrictions, unlike in many or most European countries. Note that,
in addition to typically consisting partly of dioxins, diesel emissions as a
whole are known separately to be endocrine disruptors and carcinogens. Backyard burning (including its typical major component of plastics trash, which
contributes to formation of dioxins) is difficult to control and became the
largest single source of dioxin releases in the U.S. environment as of the
latest EPA inventory (for year 2000) above source,(34)Table 1-4). The worst effects of the pollution
generated would be on infants and child-bearing women living in the areas near
where the burning is done, but the dioxins released would also enter the food
chain of the general population (this burning is mostly done in rural
areas). The emissions released would also be deposited on soil, water
supplies, and in the form of dust, to which all infants downwind could be
exposed.

Regarding the
rapidly-increasing dioxins from diesel emissions, typically reaching closely
into populated areas, those emissions are probably what basically underlie the doubled risk of autism found among infants residing within
about 1000 feet of freeways in a California study.(194)(Diesel
emissions are known to be many times higher than unleaded gasoline emissions in
dioxin content.)(198)

BPA (Bisphenol
A)is another recognized
endocrine disruptor, to which people including future mothers and nursing
mothers are especially exposed via its usein plastic packaging of
food and drinks, including in linings of metal cans. Production of BPA in the U.S. increased over 100-fold
between 1991 and 2004. The National Toxicology Program (NTP) has
“some concern” for effects on the brain, behavior, and prostate
gland in fetuses, infants, and children at current human exposures to BPA. The U.S. Geological
Survey is confident that adult exposure to BPA affects the male reproductive
tract, and that long-lasting effects in response to developmental exposure
to BPA occur in thebrain, male reproductive
system, and metabolic
processes.(38)

A review of studies of exposure of
pregnant and lactating mice to a "low, environmentally relevant dose of
BPA" found that this had observable effects in the offspring of behavioral
responses to novelty, of exploration behavior and activity in various
environments, and of sensitivity to rewards.(38a)

PBDEs have also been increasing extremely
rapidly in environments of developed countries. (See Section 1.7.1 at this link )

More on
how these toxins harm development:

In addition
to possible or known endocrine-disruption and sometimes potent mutagenic
properties of PAHs,(39)many of the derivatives, also,
"have been found to be highlymutagenic." (same
EPA source, p. 2-90)
Mutagens should be of special concern because they can affect the descendants
of a person who outwardly appears to be unaffected. Elsewhere in this paper
there are various references to possible effects of environmental toxins on
pregnant women and developing infants, and for brevity the possibleeffects on the
genetic material in future parents of both genders will not be mentioned at the same
time. But it should be kept in mind that mutagens couldbe
affecting genes of both men and women now in ways that may not be apparent in
them but which could be expressed in their future children.

A number of
studies indicate that dioxins and dioxin-like compounds (which include some
types of PCBs) decrease circulating thyroid hormone levels, which can impair
the brain development of offspring. According to the EPA's web page on
health effects of PCBs, "newborn monkeys exposed to PCBs showed
persistent and significant deficits in neurological development, including
visual recognition, short-term memory and learning. Some of these studies were
conducted using the types of PCBs most commonly found
inhuman breast milk."
"Even low levels of dioxin or PCB exposure during the perinatal period
can greatly influence neurological development" in this way and "can
cause irreversible neurological damage." (40) Most major sources of releases
of PCBs to the environment were discontinued in 1979, which helps explain the
major decline in mental impairment among girls born in recent decades.
(Mental impairment of boys resulting from PCBs would have declined also,
but that was obscured by increase in mental impairment of boys resulting from
something new that predominantly affects boys, such as autism; as PCBs
in the environment declined, other neuro-developmental toxins that are known to
specifically affect males were increasing, such as dioxins from diesel
emissions, other diesel emission components, and the especially rapidly
increasing PBDEs.) Countering the drop in PCB releases from
industrial sources, PCBs are also part of diesel emissions,(40a) which have been increasing rapidly in
the U.S., according to the EPA's latest data. PCBs are also
extremely persistent in the environment and (along with other variations of
dioxins and dioxin-like chemicals) are still very significant in
harmfulness. As of 2006, the EPA reported that "one-third of
general population TEQDFP (dioxin toxic equivalency) exposure is due
to PCBs." (41)

To
illustrate the potency of some of these developmental toxins, it is worth
considering a test performed on rhesus monkeys with Aroclor 1248, a
commonly-used commercial product that contained PCBs. According to the
U.S. ATSDR, Aroclors were “useful in a wide variety of applications, including
dielectric fluids in transformers and capacitors, heat transfer fluids, and
lubricants…. PCBs are combustible liquids, and the products of combustion may
be more hazardous than the material itself.” (43) Other common uses of PCBs
included fluorescent light ballasts and plasticizers.(44) “In rhesus monkey infants whose
mothers were or had been exposed to Aroclor 1248 during gestation and lactation,
behavioral testing showed hyperactivity and retarded learning ability…. These effects were reported at
doses of about 0.006 mg Aroclor 1248/kg bw/day to the mothers.” (45) Assuming a recognized average
weight of 5.3 kg (12 pounds) per female monkey, this works out to 0.032 mg per
monkey per day, or a dose of less than one 800,000th of
one ounce of Aroclor
per day per gestating/lactating female monkey. When considering the
effects of 1/800,000th of an ounce of a PCB-containing
product, also bear in mind that 600,000 tons of PCBs were produced in the U.S.
between 1930 and 1977, that they are very stable and are contained in
considerable equipment that is still in use (and sometimes leaking);
they are also heavily present in landfills, which are a major source of
emissions of toxins to the atmosphere (especially during fires), not to mention
the landfills’ drainage to water supplies. Although PCBs are no longer
produced in the U.S. and have recently been banned in most countries, their
continued presence in imported products is open to question. Also, indoor
air in houses with floors finished with PCB-containing wood finish have been
found to contain high levels of PCB. (46) At the rate of wide use of a
chemical for a half century or more before determining that it is too toxic (as
was the case with the pesticides endosulfan and dicofol), one may reasonably
wonder about the safety of the materials that are now being used in place of
PCBs. (Yes, most of the thousands of chemicals introduced into use
in recent decades have not been tested for safety.)

Pesticides also,
including some that are used residentially, have been widely found in breast
milk.(92).Section 1.6.a at www.pollutionaction.org/breastfeeding-and-autism-and-cancer.htm provides details about connections
between various pesticides to which fetuses and infants are exposed and (a)
autism, (b) other changes in social behavior and brain development, (c)
attention deficit disorders and hyperactivity disorders, (d) feminization of
males and (e) masculinization of females.

Bromine is another neurological toxin
excreted in breast milk;
bear in mind that a mother could absorb bromine through her skin while in a
pool or spa treated with bromine as a disinfectant.

Most of the research that has found
developmental harm to result from exposure to these chemicals was based on
tests with animals, but “the chemical structures of hormones and their
receptors are very similar among vertebrates, including humans. A chemical that
binds with an estrogen receptor in mice is almost certainly going to bind with
an estrogen receptor in people.” (93) Research with human data
has verified the results from animal tests regarding the testosterone-reducing,
de-masculinizing effects of phthalates, another toxin known to be present in
breast milk. (Section 1.6.b at www.pollutionaction.org/breastfeeding-and-autism-and-cancer.htm)

Some commentators downplay
the significance of the extraordinarily high dosage of toxins received by
infants in breast milk, pointing out that, if one looks at that dosage spread
out over a typical 70-year lifespan, it becomes a relatively minor addition to
the typical total lifetime exposure to the toxins. The problem with that
viewpoint is that permanent, life-impairing neurological damage as well as
childhood cancer can occur during infancy while effective exposure levels are
many times higher than the later lifetime average, early levels that are especially
high in relation to the infant's vulnerable stage of development.

As explained above, breast
milk today is not the beneficial, safe substance today that it was in earlier
times:
Essentially all of the above toxins have begun to become major problems in the
environment only beginning in the mid-20th-Century, with some of
them (such as PBDEs, BPA and some pesticides) not becoming significant until
very late in the 20th Century. Many new types of pesticides
were introduced only in the 1980's..(92).

Message to health professionals,
scientists, and othersreading this
paper: This author cordially invites you to indicate your reactions to
the contents presented here. As of now, new parents almost never hear
anything but completely one-sided promotion of breastfeeding, with no mention
of possible drawbacks except in cases of serious problems on the part of the
mother. If you feel that parents should be informed about both sides of
this question and thereby enabled to make an educated decision in this
important matter, please write to the author of this paper. Also, if you
find anything here that you feel isn't accurately drawn from trustworthy
sources or based on sound reasoning, please by all means send your comments, to
dm@pollutionaction.org. All comments will be posted at
the end of this paper, at ***

To return to the main page of this
website, click on the "back" arrow on your browser or click on www.babyfeeding.info .

The exact wording that was paraphrased
here was, "The proper development of many
systems and functions depends on the timely action of hormones, particularly
sex steroids; therefore, interfering with such actions can lead to a wide array
of effects that may include altered metabolic, sexual, immune, and
neurobehavioral functions. Effects of this type, that occur following exposure
during fetal life via the placenta or early in life caused by either direct
exposure to chemicals or exposure via maternal milk, are discussed in this
section."

(34a) National Academies of Science
report on dioxins in the food supply.
http://books.nap.edu/catalog.php?record_id=10763

(34b)www.epa.gov/iris/supdocs/dioxinv1sup.pdf in
section 4.3.5, at end of that section, "...the resulting RfD in standard
units is 7 × 10−10 mg/kg-day." In the EPA’s “Glossary of
Health Effects”, RfD is defined: “RfD (oral reference dose): An estimate
(with uncertainty spanning perhaps an order of magnitude) of a daily oral
exposure of a chemical to the human population (including sensitive
subpopulations) that is likely to be without risk of deleterious noncancer
effects during a lifetime.”

(34c) U.S. EPA. Estimating Exposure
To Dioxin-Like Compounds - Volume I: U.S. Environmental Protection Agency,
Washington, D.C., EPA/600/8-88/005Ca., 2002, revised 2005 – http://cfpub.epa.gov/si/si_public_record_Report.cfm?dirEntryID=43870, Section II.6, "Highly
Exposed Populations" (nursing infants are considered to be one of the
highly-exposed populations), 4/94 (p. 39) "Using these procedures
and assuming that an infant breast feeds for one year, has an average weight
during this period of 10 kg, ingests 0.8 kg/d of breast milk and that the
dioxin concentration in milk fat is 20 ppt of TEQ, the average daily dose to
the infant over this period is predicted to be about 60 pg of TEQ/kg-d."

(82) National
Academies Press: Health Risks from Dioxin and Related Compounds: Evaluation of
the EPA Reassessment (2006), Board on Environmental Studies and Toxicology,
National Academy of Sciences; the original source is not quoted directly
because it is part of a draft, not for quoting

(90a1) Quotation
to be found at
http://www.scientificamerican.com/article.cfm?id=earth-talks-breast-feeding

(90a2) The wonder
of breasts Florence Williams The Guardian, Friday 15 June 2012

(90b) Particle and
Fibre Toxicology, Effects of prenatal exposure to diesel exhaust particles on
postnatal development, behavior, genotoxicity and inflammation in mice. Karin S
Hougaard et al., National Research Centre of the Working Environment,
Copenhagen, Denmark. Published: 11 March 2008 Particle and Fibre Toxicology
2008, 5:3 doi:10.1186/1743-8977-5-3 This article is available from:
http://www.particleandfibretoxicology.com/content/5/1/3

(90c)
http://ntp.niehs.nih.gov/files/dieselexhaust.pdf

(91) CAS No:
7726-95-6) Health-based Reassessment of Administrative Occupational Exposure
Limits, Committee on Updating of Occupational Exposure Limits, a committee of
the Health Council of the Netherlands

(93) Challenged
Conceptions: Environmental Chemicals And Fertility" 2005, a publication of
Stanford University School of Medicine, p. 10

(96) An Inventory
of Sources and Environmental Releases of Dioxin-Like Compounds in the United
States for the Years 1987, 1995, and 2000", EPA/600/P-03/002F, November
2006: especially Table 1-17. 2000 appears to be the most recent year for which
the EPA provides national dioxin release data